The spontaneously hypertensive rat (SHR) is generally believed to represent the best experimental model for essential hypertensive man; as such, it provides an outstanding opportunity to perform critically important studies impossible to obtain in man, for obvious ethical considerations. Hemodynamic studies associated with myocardial and renal metabolic studies can be, but have not yet been performed in an experimental (or clinically) hypertensive situation. Our previous hemodynamic and preliminary metabolic studies in the SHR have permitted this proposal which will provide quantitative elucidation of: (1) organ and intraorgan blood flow (radioactive microspheres) in the SHR; (2) metabolic alterations of the adenylate cyclase system associated with functional hemodynamic correlates of naturally developing myocardial hypertrophy; (3) biochemical corroboration of myocardial hypertrophy and/or hyperplasia in sustained system hypertension; (4) hemodynamic and metabolic changes associated with breeding-induced "labile hypertension" from normotensive (Wistar and WKY) rats; (5) alterations of renal medullar interstitial cellular granularity with progressive hypertensive vascular disease and its correlation with juxtaglomerular cell granularity and vascular involvement; and (6) alterations of intrarenal and intramyocardial flow distribution, their associations with the renin-angiotensin-aldosterone system and adenylate cyclase activity, respectively, with antihypertensive therapy and/or regression of hypertrophy. From these studies it should be possible to understand better the relationships between progressing (or regressing) hypertensive vascular disease (as indicated by hemodynamic functions) with certain metabolic functions in two of the major target organs of this extremely common disease.